[Roles of KLF5 in inhibition TNFα-induced SK-BR-3 breast cancer cell apoptosis]

Zhonghua Yi Xue Za Zhi. 2014 Jul 8;94(26):2004-7.
[Article in Chinese]

Abstract

Objective: To explore the expression levels and roles of Krüpple-like factor 5 (KLF5) in tumor necrosis factor α (TNFα)-induced SK-BR-3 breast cancer cells.

Methods: SK-BR-3 breast cancer cells were stimulated by TNFα at different concentrations (0, 1, 5, 10, 20 µg/L) for specified durations (0, 6, 12, 24, 36 h). Western blot was performed to detect KLF5 protein levels. Then Western blot and quantitative real-time PCR (qRT-PCR) were used to detect the expression levels of apoptosis genes. Flow cytometry and qRT-PCR were used to observe the effects of exogenous KLF5 on TNFα-induced apoptosis of SK-BR-3 breast cancer cell.

Results: KLF5 expression levels significantly decreased in TNFα-stimulated SK-BR-3 breast cancer cells in a concentration- and time-dependent manner. Quantitative RT-PCR results showed that TNFα up-regulate apoptosis gene caspase 3, caspase 9 and bax expression levels and down-regulate bcl-1 level in SK-BR-3 cells. Adenovirus expression vectors of pAd-GFP and pAd-GFP-KLF5 were constructed and used to infect SK-BR-3 breast cancer cells. Over-expression of GFP-KLF5 inhibited apoptosis in TNFα-stimulated SK-BR-3 breast cancer cells.

Conclusion: TNFα reduces KLF5 expression in SK-BR-3 breast cancer cells and KLF5 participates in TNFα-induced SK-BR-3 cell apoptosis.

MeSH terms

  • Apoptosis / drug effects*
  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • Humans
  • Kruppel-Like Transcription Factors / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • KLF5 protein, human
  • Kruppel-Like Transcription Factors
  • Tumor Necrosis Factor-alpha